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Activation and Proliferation of Murine Microglia are Insensitive to Glucocorticoids in Wallerian Degeneration
Author(s) -
Castaño A.,
Lawson L. J.,
Fearn S.,
Perry V. H.
Publication year - 1996
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1996.tb01243.x
Subject(s) - microglia , wallerian degeneration , glucocorticoid receptor , axotomy , dexamethasone , biology , superior colliculus , optic nerve , microbiology and biotechnology , receptor , glucocorticoid , immunology , endocrinology , neuroscience , central nervous system , medicine , inflammation
Activation and proliferation of microglia are commonly described in the central nervous system after a wide range of insults, but the mechanisms that regulate their phenotype in vivo are still poorly understood. We have studied the effect that adrenalectomy and dexamethasone treatment have on the proliferation and activation of microglia during Wallerian degeneration of the optic nerve in BALB/c mice. We found that the onset and rate of microglia proliferation is independent of glucocorticoids. There was an increase in F4/80‐positive cells 3 days after optic nerve crush, with a peak at 7 days, both in the optic nerve and its target, the superior colliculus. The numbers of F4/80‐positive cells remained high up to 3 weeks after crush, the longest time point examined. We also found that up‐regulation of F4/80 and the complement receptor type 3 and expression of major histocompatibility complex class II antigens were not affected by adrenalectomy or dexamethasone treatment. These observations show that, unlike microglia in vitro or peripheral macrophages, microglia do not readily respond to glucocorticoids, which could indicate a lack of or reduced expression of glucocorticoid receptor in these cells.